PAPD5-mediated 3' adenylation and subsequent degradation of miR-21 is disrupted in proliferative disease

Joost Boele; Helena Persson; Jay W. ShinYuri IshizuInga S. NewieRolf S?kildeShannon M. HawkinsCristian CoarfaKazuhiro IkedaKen-ichi TakayamaKuniko Horie-InoueYoshinari AndoA. Maxwell BurroughsChihiro SasakiChizuru SuzukiMizuho SakaiShintaro AokiAyumi OgawaAkira HasegawaMarina LizioKaoru KaidaBas TeusinkPiero CarninciHarukazu SuzukiSatoshi Inoue

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PAPD5-mediated 3' adenylation and subsequent degradation of miR-21 is disrupted in proliferative disease

机译：PAPD5-mediated 3' adenylation and subsequent degradation of miR-21 is disrupted in proliferative disease

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Next-generation sequencing experiments have shown that micro- RNAs (miRNAs) are expressed in many different isoforms (isomiRs), whose biological relevance is often unclear. We found that mature miR-21, the most widely researched miRNA because of its importance in human disease, is produced in two prevalent isomiR forms that differ by 1 nt at their 3' end, and moreover that the 3' end of miR-21 is posttranscriptionally adenylated by the noncanonical poly(A) polymerase PAPD5. PAPD5 knockdown caused an increase in the miR-21 expression level, suggesting that PAPD5-mediated adenylation of miR-21 leads to its degradation. Exoribonuclease knockdown experiments followed by small-RNA sequencing suggested that PARN degrades miR-21 in the 3'-to-5' direction. In accordance with this model, microarray expression profiling demonstrated that PAPD5 knockdown results in a down-regulation of miR-21 target mRNAs. We found that disruption of the miR-21 adenylation and degradation pathway is a general feature in tumors across a wide range of tissues, as evidenced by data from The Cancer Genome Atlas, as well as in the noncancerous proliferative disease psoriasis. We conclude that PAPD5 and PARN mediate degradation of oncogenic miRNA miR-21 through a tailing and trimming process, and that this pathway is disrupted in cancer and other proliferative diseases.

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《Proceedings of the National Academy of Sciences of the United States of America》 |2014年第31期|11467-11472|共6页
作者
Joost Boele; Helena Persson; Jay W. ShinYuri IshizuInga S. NewieRolf S?kildeShannon M. HawkinsCristian CoarfaKazuhiro IkedaKen-ichi TakayamaKuniko Horie-InoueYoshinari AndoA. Maxwell BurroughsChihiro SasakiChizuru SuzukiMizuho SakaiShintaro AokiAyumi OgawaAkira HasegawaMarina LizioKaoru KaidaBas TeusinkPiero CarninciHarukazu SuzukiSatoshi Inoue;
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作者单位

Department of Obstetrics and Gynecology and Center for Reproductive Medicine, Baylor College of Medicine, Houston, TX 77030;

Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030;

Division of Gene Regulation and Signal Transduction, Research Center for Genomic Medicine, Saitama Medical University, Saitama 350-1241, JapanDepartments of Anti-Aging Medicine, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-8655, JapanRIKEN Omics Science Center, Yokohama, Kanagawa 230-0045, JapanDepartment of Systems Bioinformatics, Amsterdam Institute for Molecules, Medicines and Systems, VU University Amsterdam, 1081 HV, Amsterdam, The NetherlandsDepartment of Biosciences and Nutrition, Karolinska Institutet, SE-141 83 Huddinge, SwedenDivision of Oncology, Department of Clinical Sciences, Lund University Cancer Center/Medicon Village, SE-223 81 Lund, Sweden;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种英语
中图分类自然科学总论;
关键词
nucleotidyl transferase; microRNA processing;

PAPD5-mediated 3' adenylation and subsequent degradation of miR-21 is disrupted in proliferative disease

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